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[Renal osteodystrophy(II)].

Renal bone disease represents one of the major complications of end-stage renal disease, accounting for the numerous and various changes at bone level, determined by abnormal calcium and phosphorus homeostasis and by changes in calcitriol and PTH synthesis. PTH represents as well a major uraemic toxin, exerting profound systemic effects, particularly at the cardiovascular level. PTH synthesis is mainly controlled by changes in calcium-phosphorus balance and calcitriol production by the kidneys. Several others factors are important in the development of secondary hyperparathyroidism: acidosis, autonomisation of PTH secretion and peripheral (target-organ) resistance to PTH actions. Although bone biopsy represents the definitive diagnostic test to differentiate between osteitis fibrosa, low-turnover bone disease and bone involvement unrelated to disturbed calcium metabolism (i.e. beta 2-microglobulin-related amyloidosis), plasma intact PTH generally exhibits a reasonably good relation with bone histology parameters. Moreover serum bone-specific alkaline phosphatase isoenzyme, serum pyridinoline and the novel serum markers for bone turnover are highly specific and correlate with bone histomorphometry parameters, so that, preventive and therapeutic strategies should be re-evaluated based solely on biochemical parameters.

Chronic Kidney Disease-Mineral and Bone Disorder↗

PubMed2002

Vitamin D deficiency and severe hyperparathyroidism.

The typical manifestations of severe hypercalcemia with osteitis fibrosa cystica have become exceedingly rare. We describe the case of a woman hospitalized for a tibial tumor with functional impotence, leading to a diagnosis of primary hyperparathyroidism (HPT I) associated with profound vitamin D deficiency. This 31-year-old woman was admitted, after two pregnancies complicated by the HELLP syndrome. Preoperative laboratory values were as follows: calcemia 4.05 mmol/l (2.2-2.6); urinary calcium 30 mmol/24 h (1.25-7.5); parathormone (PTH) 1 195 pg/ml (10-60); and 25 OH-vitamin D 13 nmol/l (22-120). Specific MIBI uptake by the tibial lesion oriented the diagnosis towards a brown tumor. After surgical excision of a parathyroid adenoma and the brown tumor (associated with tibial fracture), calcemia fell to 1.55 mmol/l and normalized after three months. Urinary calcium fell to 0.1 mmol/24 h and remained low during the 2 years following surgery. Vitamin D levels rapidly normalized on supplementation (87 nmol/l). PTH levels fell markedly after surgery but remained higher than normal till 2 years after surgery despite normalization of calcemia three months after. Bone repair, estimated by means of bone densitometry, improved from preoperative Z-score values of - 6.54, - 5.20 and - 3.50 in the left femoral neck, right femoral neck and lumbar spine, respectively, to - 0.20, - 1.55 and - 0.28, respectively, one year after surgery. In conclusion, this case illustrates: 1) the severe osseous expression of HPT probably related to vitamin D deficiency; 2) specific MIBI uptake by the bone lesion, orientating the diagnosis towards a brown tumor; 3) the consequences of vitamin D deficiency on postoperative outcome, with transient severe initial hypocalcemia related to bone calcium avidity; 4) a possible link between HPT and the HELLP syndrome.

Adult↗

PubMed1992

Calcitriol injection for the management of renal osteodystrophy.

The introduction of synthetically produced calcitriol in the early 1970s was an important contribution to the prevention and treatment of renal bone disease. However, despite the efficacy and the availability of oral calcitriol many dialysis patients continued to develop secondary hyperparathyroidism (Norris, 1991). Effective treatment was often impossible in patients with osteitis fibrosa because even low oral doses of calcitriol could cause hypercalcemia (Andress, Norris, Coburn, Slatopolsky, & Sherrad, 1989). From 1981 to the present, numerous studies have been conducted that have demonstrated intravenous calcitriol as being more effective and having several advantages over the oral route of administration, particularly in patients with poor compliance and those with a tendency to develop hypercalcemia.

Calcitriol↗

PubMed1992

[Renal osteodystrophy in Maracaibo].

In the present work we report the bone histologies obtained from the iliac crest of 49 patients on chronic hemodialysis in Maracaibo. All of them were dialyzed thrice weekly with untreated tap water containing high aluminum (Al) levels. Their mean blood Al levels were found to be higher than 100 micrograms/L. Histomorphometry was used for the diagnosis of the underlying renal osteodystrophic type. Al-staining techniques (Aluminum) were applied for detection of bone Al deposits. Additionally, bone Al content was determined quantitatively by means of graphite furnace atomic absorption spectroscopy. A mixed type of osteodystrophy (type III according to Delling's classification) consisting in the simultaneous presence of hyperparathyroid bone lesions (osteitis fibrosa, OF) and a hyperosteoidosis (osteomalacia, OM) was found in 63.3% of the studied patients. The other patients (37.7%) exhibited a pure osteomalacia (OM). Bone Al deposits at the mineralization front were observed in 70% of cases and were frequently associated with bone pain, spontaneous fractures and skeletal deformities. We conclude that bone biopsy should be performed in all patients presenting bone pain and high blood Al levels.

Adolescent↗

PubMed1992

Effect of chronic intravenous calcitriol on parathyroid function and set point of calcium in dialysis patients with refractory secondary hyperparathyroidism.

This study evaluates the effect of intravenous calcitriol on parathyroid function and ionized calcium-PTH sigmoidal curve obtained during low- and high-calcium haemodialysis in 10 patients with osteitis fibrosa whose secondary hyperparathyroidism was refractory to conventional therapy. After 4 months of intravenous calcitriol, serum ionized calcium increased from 1.28 +/- 0.08 to 1.37 +/- 0.11 mmol/l (P less than 0.001), serum phosphate from 1.54 +/- 0.18 to 1.79 +/- 0.4 mmol/l (P NS), serum calcitriol from 16.7 +/- 9.9 to 34.3 +/- 6.4 pg/ml (P less than 0.001), while alkaline phosphatase decreased from 366 +/- 340 to 226 +/- 180 IU/l (P less than 0.05), osteocalcin from 46.4 +/- 20 to 34.5 +/- 15.3 ng/ml (P less than 0.05), and basal intact PTH from 1069 +/- 700 to 305 +/- 270 (P less than 0.01). Basal PTH started to decrease after 1 month of treatment prior to the increase in the ionized calcium. Because of hypercalcaemia the dialysate calcium was decreased from 1.75 to 1.5 mmol/l in three of five patients on haemodialysis, and calcium-containing solutions were replaced by calcium-free fluids in four of five patients on haemodiafiltration. Calcitriol dose, at the first month of therapy was 5.6 +/- 0.8 micrograms/week, but it was successively decreased because of hypercalcaemia to a final dose of 3.6 +/- 1.3 micrograms/week. After intravenous calcitriol the ionized calcium-PTH sigmoidal curve shifted to the left and downward. Maximally stimulated PTH and maximally inhibited PTH obtained during low- and high-calcium dialysis significantly decreased, as well as the ratio of basal PTH/PTHmax and the set point of calcium.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcitriol↗

PubMed1961

Chronic renal failure. Its effect on calcium, phosphorus and osseous metabolism unified approach.

The renal osteodystrophies represent the metabolic consequences of (1) vitamin D resistance, (2) secondary hyperplasia of the parathyroids, and (3) the changes in serum PO(4)= and Ca++ secondary to the renal insufficiency per se. The osseous lesion in any given patient with chronic renal failure may be osteitis fibrosa, rickets (osteomalacia), calcium deficiency osteoporosis or any combination of these. The concentration of Ca++ and PO(4)= in the serum is determined by the degree of renal failure and the skeletal response to parathyroid hormone.

Bone and Bones↗

PubMed1992

[A case of hyperparathyroid bone disease and the review of renal osteodystrophy].

We report here a typical case of hyperparathyroid bone disease associated with CRF on maintenance HD and review on Renal Osteodystrophy. A 39 year-old female patient was admitted because of polyarthralgia and pruritus. She had a history of HD due to CGN for about 13 years. Laboratory data showed an increase in serum PTH and Alkaline phosphatase level. The evidence of osteitis fibrosa was revealed by bone Xp and scintigraphy. Enlarged solid masses were found in her neck by echogram and parathyroid scintigraphy. She was diagnosed as hyperparathyroid bone disease and total parathyroidectomy c autoplantation was done. Shortly after the surgical treatment, subjective symptoms were relieved and PTH level was normalized. The bone Xp findings improved gradually.

Adult↗

PubMed1992

Use of alkaline calcium salts as phosphate binder in uremic patients.

In order to prevent aluminum toxicity induced by the association of aluminum phosphate binder with 1 alpha(OH) vitamin D3 derivatives and the use of deferoxamine with its own hazards to diagnose and treat this toxicity, we have shown in 1982 that it was possible to replace the iatrogenic association of aluminum phosphate binder with 1 alpha OH vitamin D derivatives by oral calcium carbonate taken with the meals in order to bind phosphate and correct the negative calcium balance. This led to the disappearance of the crippling aluminic osteomalacia and adynamic bone diseases in our center. The effectiveness of CaCO3 without 1 alpha(OH)D3 derivatives in the control of hyperparathyroidism in dialysis patients has been proven by the appearance in four patients of our dialysis population of an histological idiopathic adynamic bone disease associated with relative hypoparathyroidism, and by the finding that more than 50% of our dialysis population treated by this sole treatment have plasma concentration of intact PTH below twice the upper limit of normal (that is, the threshold above which only significant histological osteitis fibrosa is observed). Besides the compliance problem, the limit of CaCO3 is the occurrence of hypercalcemia which occurs in about 8% of the measurements. Since calcium acetate binds twice as much phosphate for the same dose of elemental calcium as CaCO3, its use has been recommended. However, clinical experience has shown that in spite of the fact that half the dose of calcium element given as acetate does actually control predialysis plasma phosphate as well as CaCO3, the incidence of hypercalcemia is not decreased, probably because calcium availability at the alkaline pH of the intestine is much greater with Ca acetate. When hypercalcemia is frequent (and not explained by autonomized hyperparathyroidism, adynamic bone disease, overtreatment with vitamin D, granulomatosis or neoplasia) it is necessary either to decrease the dose of calcium and complete the necessary binding of phosphate by adding small doses of Mg(OH)2 or Mg carbonate, provided the dialysate Mg is decreased to 0.2 to 0.35 mmol/liter to prevent hypermagnesemia or to decrease the dialysate calcium (DCa) concentration. The decrease of DCa can be made either just when hypercalcemia occurs or on a systemic basis according to the amount of CaCO3 used and to the necessity of associating 1 alpha(OH) vitamin D3 derivatives.(ABSTRACT TRUNCATED AT 400 WORDS)

Aluminum↗

PubMed2004

Hyperparathyroidism.

Hyperparathyroidism is a disease characterized by hypercalcemia with hypophosphoremia resulting from increased secretion of parathyroid hormone (PTH). The disease may be divided into 3 forms: a) primary, b) secondary, c) tertiary (secondary refractory form). Primary hyperparathyroidism is rare in children; hyperplasia is more frequent during the early years of life (neonates and infants) and is difficult to distinguish from adenoma in children. The disease may be asymptomatic; elevated calcemia levels (>12 <13.5 mg/dl) are accompanied by anorexia, asthenia and persistent stipsis; severely elevated concentrations (>13.5 mg/dl) are accompanied by nausea, vomiting, polyuria due to osmosis, with dehydration and progressive onset of lethargy, stupor and coma. Osteopenia or osteitis fibrosa cystica may be present due to augmented bone resorption. Height and weight increases are altered due to anorexia and dehydration. Differential diagnosis includes iatrogenic causes of hypercalcemia (excessive vitamin D intake, prolonged immobilization, etc.) and idiopathic familial hypercalcemia. Emergency treatment is required in cases of extremely elevated hypercalcemia (Ca >13.5-14 mg/dl), due to risk of injury to the heart, the central nervous system, the gastrointestinal tract and the kidneys. The 4 cardinal points of treatment are: hydration, calciuresis, inhibition of bone calcium resorption, treatment of the cause underlying hyperparathyroidism. Secondary hyperparathyroidism is found in cases where chronic hypocalcemia is present, particularly in chronic renal failure, untreated deficiency rickets, chronic intestinal malabsorption, hepatobiliary disease, types I and II vitamin D-dependent rickets, tubular acidosis or Fanconi's syndrome. The tertiary form is distinguished by the autonomous nature of the parathyroid glands which have become hypertrophic/hyperplastic due to uncontrollable, chronic severe renal failure. It can also be of iatrogenic origin due to excessive intake of inorganic phosphates in familial hypophosphatemic rickets or chronic vitamin D deficiency.

Calcium↗

PubMed2004

Histologic evolution of bone disease 6 months after successful kidney transplantation.

BACKGROUND: The histologic patterns of bone disease, as well as the evolution of renal osteodystrophy after kidney transplantation (Tx), are not well defined. Information in this regard is scarce and contradictory. METHODS: Before and 6 months after Tx, analysis of biochemical, hormonal, and bone histomorphometric parameters were performed. Twenty patients (14 men and 6 women) entered the study. Median age was 36.5 (range, 20 to 55) years, and median time on dialysis was 22 (9 to 88) months. RESULTS: Bone histomorphometric diagnoses at pre-Tx were adynamic bone disease, 12; mixed bone disease, 3; mild disease, 3; and osteitis fibrosa, 2. After Tx, 11 had adynamic bone disease; 8, mild disease; and 1, osteomalacia. As a whole, dynamic parameters improved significantly in patients who had adynamic bone. Five of the 12 with this diagnosis completely recovered their bone turnover. Pre-Tx hyperparathyroidism bone features improved or resolved, but 5 of the 8 patients had low-turnover bone disease (adynamic disease, 4; osteomalacia, 1). Three of them had persistence of aluminum and/or iron deposits on bone surface, and the other 2 had hypophosphatemia and high intact parathyroid hormone levels. Overall, biochemical parameters tended toward normalization. Serum intact parathyroid hormone before Tx was correlated negatively with post-Tx trabecular thickness. CONCLUSION: Six months after Tx, bone histology remained abnormal. The high turnover bone disease improved in all cases, but in most of them low turnover bone disease emerged. Nearly half of the cases with pre-Tx adynamic bone disease recovered their bone turnover completely with some improvement observed in the majority of the remaining cases.

Adult↗

PubMed2004

[Pathogenesis of secondary hyperparathyroidism and renal bone disease].

Patients with chronic renal disease (CKD)almost always develop secondary hyperparathyroidism (SHPT) due to hypocalcemia, phosphate retention, and abnormalities in vitamin D (VD) metabolism. Concomitant decreases in VD receptor and calcium sensing receptor in the parathyroid glands render them more resistant to the action of VD and calcium, and accelerate parathyroid cell growth. Several types of bone diseases are known to occur in CKD patients. Excessive secretion of parathyroid hormone (PTH) due to SHPT causes high-turnover bone disease, called osteitis fibrosa. Among low-turnover bone disease (LTBD), osteomalacia which is characterized by calcification defect is often complicated with VD deficiency and/or aluminum accumulation. Recently, frequency of adynamic bone disease caused by PTH suppression, another type of LTBD, is increasing probably due to calcium salts as phosphate binder with or without VD treatment.

Aluminum↗

PubMed2004

[Diagnosis and classification of renal osteodystrophy].

Bone histomorphometry is essential to diagnosis of renal osteodystrophy. Sherrard et al classified renal osteodystrophy into the 5 groups according to Fb.V/TV, OV/BV and BFR/TV of cancellous bone (Osteitis fibrosa, Mixed uremic osteodystrophy, Osteomalacia, Mild lesion, Aplastic disease). In addition, because endocortical bone loss is generally irreversible, the evaluation of this region in the transiliac bone biopsy specimen also seems to be important.

Bone and Bones↗

PubMed2003

[Bone mass measurement and its evaluation: their usefulness and problem].

In this paper, bone mass measurement and its evaluation have been reviewed. The bone lesions in renal osteodystrophy are classified into high- and low turnover, and the decreased rate of bone mineral density (BMD) might be different in osteitis fibrosa and adynamic bone disease. Secondary hyperparathyroid patients showed lower BMD values in mainly composed of the cortical bone than those in mainly composed of the trabecular bone.

English Abstract↗

PubMed2003

[Renal osteodystrophy and vitamin D].

Vitamin D deficiency is one of major pathogeneses of renal osteodystrophy (ROD). Vitamin D deficiency produces osteitis fibrosa via secondary hyperparathyroidism and osteomalacia via hypocalcemia. To prevent and treat ROD, vitamin D supplementation is an inevitable tool. Recent progresses of vitamin D therapy including development of new vitamin D analogues and direct injection to parathyroid gland will contribute to the successful treatment of ROD.

English Abstract↗

PubMed2003

[Parathyroidectomy for patients with renal osteodystrophy].

It has been proposed that we should focus our attention on prevention of cardiovascular complication rather than to prevent osteitis fibrosa as the purpose to control secondary hyperparathyroidism (2HPT) induced by chronic renal failure. Active vitamin D and these analogues influence the bone turnover in hemodialysis patients and recently we often encounter the patients whose bone turnover is not high in spite of high PTH level. The aim of parathyroidectomy is gradually changed from improvement of bone disease to reduce high PTH level to prevent cardiovascular complication and extraskeletal symptoms. When it is difficult to control high PTH level without increase of calcium phosphate product, parathyroidectomy should be chosen.

English Abstract↗

PubMed2002

[Clinical effect of parathyroidectomy for advanced renal hyperparathyroidism].

Advanced renal hyperparathyroidism induced not only osteitis fibrosa but also vessel and valvular calcification which affect high mortality due to cardiovascular disease. Parathyroidectomy usually promises dramatic clinical improvement of hyperparathyroidism. However, ectopic calcification except for tumor calcinosis is irreversible by parathyroidectomy. Then the surgery should be indicated at right time. Total parathyroidectomy with forearm autograft is suitable operative method for renal hyperparathyroidism, because removal of autograft can be less invasively performed at recurrence which is not negligible after the internal operation.

English Abstract↗

PubMed2005

Parathyroid carcinoma: a case series.

INTRODUCTION: We present 3 patients with parathyroid carcinoma and describe their presentations, clinical profiles, and management. MATERIALS AND METHODS: A case series review of medical records. RESULTS: Two women and 1 man (age range, 32 to 57 years) had parathyroid cancer and primary hyperparathyroidism (PHPT). One patient presented with osteitis fibrosa, 1 with renal stone and a neck mass, and 1 with recurrence of PHPT after excision of supposedly benign parathyroid adenoma 4 years ago. All had severe hypercalcaemia and elevated parathyroid hormone levels that ranged from 4 to 43 times above the normal range. Exploration of the neck clearly identified 1 parathyroid tumour with local invasion; 2 other specimens showed capsular and vascular invasion on frozen section and final histology. All 3 patients underwent parathyroidectomy and ipsilateral hemithyroidectomy. Parathyroid size ranged from 1.3 to 4 cm and no lymph node metastasis was identified. No patient had tumour recurrence after a follow-up period of 1 year. CONCLUSION: Parathyroid carcinoma is a rare endocrine malignancy. Suspicious features include marked hypercalcaemia, neck mass, and local recurrence. Parathyroidectomy with ipsilateral hemithyroidectomy and nodal clearance gives the best chance of reducing local tumour recurrence.

Adult↗

PubMed1991

Renal osteodystrophy.

The term "renal osteodystrophy" is used to include skeletal disorders of patients with chronic renal failure: osteitis fibrosa, osteomalacia, osteosclerosis, osteoporosis and the frequently associated extraskeletal calcifications. It is the chronic glomerular disease with phosphate retention and resultant hyperphosphatemia on one hand and deficient 1,25 (OH)2 D3 and resultant hypocalcemia on the other to induce secondary hyperparathyroidism. The three most common causes of chronic renal failure in our patients are chronic glomerulonephritis, diabetic nephropathy, hypertensive nephropathy in decreasing frequency, polycystic renal disease occurs in five patients. Other miscellaneous causes include nephrotic syndrome, chronic pyelonephritis, systemic lupus erythematosus, periarteritis nodosa, interstitial nephritis and renal stones. The bone changes are similar in primary and secondary hyperparathyroidism and the incidence of brown tumor is about 3% in the former and 1.5 to 1.7% in the latter. We present one among the 94 dialyzed patients who has long-standing severe chronic renal failure from polycystic kidney disease and develops brown tumor in the mid ulna after 7 years on maintenance hemodialysis. The incidence of brown tumor in our series is about 1.1%. Because of increased longevity of the dialyzed patients, brown tumor from secondary hyperparathyroidism is now more commonly observed. Hyperphosphatemia with serum calcium-phosphate products exceeding plasma solubility of 60 to 75 mg/dl may induce soft tissue and vascular calcification. This explains the much higher incidence of soft tissue calcification in secondary than primary hyperparathyroidism; two of our patients with generalized Monckeberg's type arterial calcification and multiple periarticular calcifications in five patients have been observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗